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[Multiple lines of evidence now support this hypothesis: 1) intracerebroventricular (icv) OT administration inhibits food intake in fasted rats and NaCl intake in hypovolemic rats; 2) icv administration of OT-receptor antagonists significantly blunts the effects of anorexigenic agents on food intake and the action of naloxone to inhibit hypovolemia-induced intake of NaCl, but not water; 3) most treatments that inhibit food and/or NaCl intake stimulate expression of c-fos in parvocellular as well as magnocellular OT neurons, indicating simultaneous activation of both centrally-projecting and pituitary-projecting OT neurons; 4) icv treatment with cytotoxic conjugates of ricin A and OT to disable cells bearing OT receptors leads to a disinhibition of NaCl intake similar to that produced by OT antagonists; 5) administration of ethanol, a well known inhibitor of OT secretion, produces effects on stimulated food and NaCl intake in rats analogous to those produced by OT-antagonists and ricin-OT conjugates.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine.
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